Physiology Unit 4 - Blood - Fofi
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| Fluids of the body | blood and interstitial fluid
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| Composed of plasma, variety of cells | blood
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| Bathes cells of the body | interstitial fluid
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| Flow of nutrients and oxygen | blood to the interstitial fluid to the cells
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| Flow of wastes | cells to interstitial fluid to blood
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| Functions of blood | transportation of O2, CO2, metabolic waste, nutrients, heat, hormones; regulation of pH via buffers, regulation of body temperature; protection from disease and loss of blood
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| Physical characteristics of blood | more viscous than water, pH of 7.4 (7.35 to 7.45); 5 to 6 L in average male; 4-5 L in average female; hormonal negative feedback systems maintain constant blood volume and pressure
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| Components of blood | 55% plasma, 45% RBCs, <1% WBCs, platelets
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| Components of plasma | 90% water, 7% plasma proteins
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| Hematocrit | is the percentage of blood volume occupied by RBCs; female range is average of 42%; male average is 45%
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| Anemia | condition due to not enough RBCs
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| Polycythemia | condition due to too many RBCs
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| Normal hemoglobin range | females are 12-16 g/100ml of blood; males are 13.5-18
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| Blood plasma | over 90% water, 7% plasma proteins, 2% other substances (electrolytes, hormones, gases, waste)
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| Plasma proteins | created in liver, confined to the bloodstream; consist of albumin, globulins, and fibrinogen
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| Albumin | plasma protein; contributes to blood osmotic pressure, used for transport
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| Globulin | plasma protein; contributes to defense against foreign particles
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| Fibrinogen | plasma protein; contributes to clotting
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| Formed elements of blood | RBCs, WBCs, platelets
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| White blood cells (leukocytes) | granular—neutrophils, eosinophils, basophils; agranular—lymphocytes, monocytes
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| Normal RBC count | 5 million/drop
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| Normal WBC count | 5-10,000
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| Platelet count | 150,000-400,000
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| Blood cell formation | occurs only in red marrow of flat bones like sternum, ribs, skull, pelvis, ends of long bones; most types need to be continually replaced because they die within weeks or days
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| Red blood cells | contain oxygen carrying protein hemoglobin
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| Red blood cell shape | bioconcave disk
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| How does RBC cell shape link its function? | bioconcave disk shape gives increased surface area/volume ratio, allows for flexibility to pass through narrow passages, it has no nucleus or organelles, and no mitochondrial ATP formation
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| Hemoglobin | globin protein consisting of 4 polypeptide chains; each chain has one heme pigment; each heme contains one iron ion that can combine with one oxygen molecule.
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| Hemoglobin function | each can carry four oxygen molecules; acts as a buffer and balances pH of blood; transports 23% of total CO2 waste from tissue cells to lungs for release
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| Hemoglobin ranges | females—12-16g/100mL of blood; males 13.5-18g
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| RBC life cycle | usually only live 120 days; wear out from bending through capillaries, no repair possible due to lack of organelles; worn out cells removed by macrophages in spleen and liver
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| Processing of “retired” RBCs | removed from circulation by macrophages in spleen/liver; globin portion broken into amino acids; recycled to make new proteins; heme portion split into iron & biliverdin which is converted into bilirubin; bilirubin secreted by liver into bile and excreted
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| Erythropoiesis | production of RBCs; proerythroblast starts to produce hemoglobin; nucleus ejected, reticulocyte is formed, escapes from bone marrow into blood; ejects organelles, matures into RBC; factors required are erythropoietin (kidneys), vitamin B12, iron
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| Erythropoiesis | stimulus--tissue hypoxia; kidneys detect reduced O2 capacity of blood, release erythropoietin; e.poietin catalyzes proerythroblast dev in red marrow into reticulocytes; more reticulocytes enter blood and become erythrocytes; O2 carrying capacity increases
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| White blood cell | less numerous than RBCs; only 2% of population is circulating blood at any given time; rest remain in lymphatic fluid, skin, lungs, lymph nodes, spleen; requires colony stimulating factor
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| Neutrophil | fastest response of all WBC to bacteria and parasites; direct actions against bacteria—release lysozymes, release defensing proteins that act like antibiotics, release strong oxidants that destroy bacteria
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| Basophil | WBC involved in inflammatory and allergy reactions; leave capillaries and enter connective tissue as mast cells; release heparin (anticoagulant), histamine, serotonin; heighten inflammatory response, account for hypersensitivity reactions
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| Eosinophil | WBC; leaves capillaries to enter tissue fluid; release histaminase, slows down inflammation; attack parasitic worms, phagocytize antibody-antigen complexes
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| Monocyte | WBC; takes longer to get to site of infection, but arrives in larger numbers; become wandering macrophages once they leave capillaries; destroy microbes, clean up dead tissue following an immune response
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| Lymphocyte | WBC B/T cells; B—destroy bacteria, their toxins, turn into plasma cells that produce antibodies; T—attack viruses, fungi, transplanted organs, cancer cells; natural—attack many dif microbes, some tumor cells; destroy foreign invaders by direct attack
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| Differential WBC count | detection of changes in numbers of circulating WBCs; indicates infection, poisoning, leukemia, chemotherapy, parasites, or allergic reaction
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| Normal WBC counts | N 60-70%; L 20-25%; M 3-8%; E 2-4%; B <1%
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| Platelet/thrombocyte | disc-shaped cell fragment with no nucleus; normal count is 150,000-400,000/drop blood; form in marrow; short life span; aged ones removed by fixed macrophages in spleen; release ADP and other chemicals needed for platelet plug formation
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| Platelet formation | formed in marrow; myeloid stem cells eventually become megakaryocytes whose cell fragments form platelets
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| Hemostasis | stoppage of bleeding in a quick and localized fashion when blood vessels are damaged; prevents hemorrhage; methods—vascular spasm, platelet plug formation, blood clotting
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| Vascular spasm | damage to blood vessel stimulates pain receptors; reflex contraction of smooth muscle of small blood vessels; can reduce blood loss for several hours until other mechanisms take over; only for small blood vessel/arteriole
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| Platelet plug formation | platelet adhesion, platelet release action, platelet aggregation
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| Platelet adhesion | platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall
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| Platelet release action | activated platelets extend projections to make contact to other platelets; release thromboxane A2, serotonin, ADP—activating other platelets; thromboxane A2 & serotonin vasoconstrict and ADP causes stickiness activating other platelets
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| Platelet aggregation | activated platelets stick together and activate new platelets to form a mass called platelet plug; plug is reinforced by fibrin threads formed during clotting process
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| Blood clotting/coagulation | substances required are Ca++, enzymes made by liver cells (clotting factors), substances released by platelets/damaged tissues; cascade of reactions in which clotting factor activates next in fixed sequence resulting in formation of fibrin threads
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| Coagulation | reactions in which blood is transformed from liquid to gel; follows extrinsic and intrinsic pathways; final three steps—prothrombin activator formed, prothrombin converted to thrombin, thrombin catalyzes polymerization of fibrinogen into fibrin mesh.
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| Pathways to prothrombin activator | initiated by intrinsic/extrinsic pathway; triggered by tissue damaging events; involves series of procoagulants, each pathway cascades toward factor X; activation of factor X—it then complexes w/ Ca ions, PF3, and Factor V to form prothrombin activator
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| Intrinsic pathway | several min; Damaged endothelium activates FXII; Platelet contacts damaged endo, release Platelet FactorIII (PF3); FXII & PF3 + Ca2+ & Clotting factors 8 & 9--creates FX activator complex--activates FX--complexes with Ca2+, PF3 & FV, forms prothrombinase
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| Extrinsic pathway | takes seconds; damaged tissue leaks tissue factor thromboplastin into blood; activates FVII, which combines w/ Ca2 & clotting FVII to make FVII tissue factor complex, which activates FX, which complexes w/ Ca2, PF3, FV to make prothrominase
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| Common pathway | prothrominase+Ca2 catalyze prothrombin to thrombin; thrombin+Ca2 catalyze fibrinogen into fibrin; fibrin strands form basis of clot; fibrin causes plasma to be gel trap; fibrin+Ca2 activate FXIII that crosslinks fibrin mesh, strengthens/stabilizes clot
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| Clot dissolution | heparin acts as anticoagulant; plasminogen becomes plasmin, fibrinolytic enzyme that dissolves small clots at site of completed repair; clot formation remains localized
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| Thrombosis | clot formed in unbroken blood vessel; attached to rough inner lining of BV; slow flowing blood allows clot factors to build up and cause coagulation; may dissolve and travel
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| Embolus | free floating clot in blood; may cause strokes, myocardial infarctions; low dose aspirin can help prevent this
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| Blood group/type | determined by presence/absence of surface antigens; glycoproteins, glycolipids; antigens A, B, and Rh(D); antibodies in plasma; cross reactions occur when antigens meet antibodies
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| Blood type A | surface antigen for A, anti-B antibodies
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| Blood type B | surface antigen for B, anti-A antibodies
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| Blood type AB | surface antigen for A and B; no antibodies
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| Blood type O | no surface antigen; antibodies for both anti-A and anti-B
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| RH blood groups | Pple w/ Rh isoantigens on RBC surface--Rh+; Normal plasma has no anti-Rh antibodies; Antibodies develop only in Rh- blood type & only w/ exposure to antigen; Transfusion reaction upon 2nd exposure to antigen results in hemolysis of the RBCs
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| Rh and moms | Rh negative mom & Rh+ fetus will mix blood @ birth; Mom's body creates Rh antibodies unless she gets RhoGam shot after first delivery, miscarriage or abortion; In 2nd child, Hemolytic Disease of the Newborn may develop causing hemolysis of the fetal RBCs
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| Universal Donors and Recipients | AB blood “universal recipients” since no antibodies in plasma, only true if cross match the blood for other antigens; type O blood “universal donors” since have no antigens on cells; theoretically can be given to anyone
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| iron-deficiency anemia | lack of absorption or loss of iron
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| pernicious anemia | lack of intrinsic factor for B12 absorption
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| hemorrhagic anemia | loss of RBCs due to bleeding (ulcer)
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| hemolytic anemia | defects in cell membranes cause rupture
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| thalassemia anemia | hereditary deficiency of hemoglobin
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| aplastic anemia | destruction of bone marrow (radiation/toxins)
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